This review provides insight into a limited number of genes known to be frequently altered in MPM, INK4 locus and
NF2, and a larger number of candidates that may play a role in MPM carcinogenesis, especially those involved in various signaling pathways.
NF2 FISH showed no case of
NF2 deletion in 17 evaluable cases.
[24] found a higher percentage of the
NF2 mutations in young patients (age under 20) with 66.7% of 12 patients compared to 34.5% of 145 adult patients.
The hallmarks of
NF2 are schwannomas, meningiomas, and ependymomas.
Additionally,
NF2 gene mutations along with a reduced merlin expression are correlated with increased Yes-associated protein (YAP) which is involved in the regulation of the arachnoid cells proliferation rate [50, 52].
Filter Name Filtering Parameter 1 NF1 IP 2
NF2 IP COUNT 3 NF3 PORT NUMBER 4 NF4 PORT DISTRIBUTION 5 NF5 PACKET COUNT 6 NF6 STACK BYTES 7 NF7 PACKETS A-> B 8 NF8 PACKETS B->A 9 NF9 BYTES A->B 10 NF10 BYTES B->A 11 NF11 DURATION 12 NF12 ABSOLUTE TIME 13 SF1 PERIPHERAL STATUS 14 SF2 UNLISTED PROCESS 15 SF3 FLAWLESS USER LOGIN 16 SF4 SUSPICIUOS TIME 17 SF5 DISK ACTIVITY 18 SF6 PORT BINDING 19 LF FIN FIN FLAG 20 LF SYN SYN FLAG 21 LF TCP CONN() TCP CONN() FLAG 22 LF NULL NULL FLAG 23 LF PING ICMP FLAG 24 LF VERSION DETECTION VER FLAG 25 LF UDP SCAN UDP FLAG 26 LF BULK SCAN BULKFLAG 27 LF WINDOWS SCAN WIN SCAN FLAG 28 LF RPC SCAN RPC FLAG 29 LF LIST SCAN LSTFLAG 30 LF IDLE SCAN IDL FLAG 31 LF FTP BOUNCE BOUNCE FLAG TABLE II.
The patient has a past medical history of
NF2, with bilateral acoustic neuromas (also known as vestibular schwannomas), diagnosed more than 10 years ago.
According to Figure 2D, the treatments with 40 (
NF2), 80 (NF3) and 180 kg [ha.sup.-1] of N (NF5) promoted a maximum SPAD index of approximately 48, which is only 4% inferior to that of the treatment with 120 kg [ha.sup.-1] of N (NF4), which was equal to 50.
Update on long-term results with auditory brainstem implants in
NF2 patients.
We report a case ofplexiform schwannoma of the posterior pharyngeal wall that occurred in a 37-year-old man who had been previously diagnosed with neurofibromatosis type 2 (
NF2).
[6] Human genes: EGFR, epidermal growth factor receptor; KRAS, Kirsten rat sarcoma viral oncogene homolog; TP53, tumor protein p53;
NF2, neurofibromin 2 (merlin); AKT1, v-akt murine thymoma viral oncogene homolog 1; BRAF, B-Raf proto-oncogene, serine/ threonine kinase; NRAS, neuroblastoma RAS viral (v-ras) oncogene homolog; KMT2D, lysine (K)-specific methyltransferase 2D; NSD1, nuclear receptor binding SET domain protein 1; CREB3L1, cAMP responsive element binding protein 3-like 1; TPR, translocated promoter region, nuclear basket protein; TSC2, tuberous sclerosis 2.